Mitochondrial Reactive Oxygen Species Production Mediated by Romo1 Expression

Young Do Yoo

doi:10.7599/hmr.2013.33.2.90

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Yoo: Mitochondrial Reactive Oxygen Species Production Mediated by Romo1 Expression

Review Article

Hanyang Medical Reviews 2013; 33(2): 90-96.

Published online: 23 May 2013

DOI: https://doi.org/10.7599/hmr.2013.33.2.90

Mitochondrial Reactive Oxygen Species Production Mediated by Romo1 Expression

Young Do Yoo

Laboratory of Molecular Cell Biology, Graduate School of Medicine, Korea University College of Medicine, Seoul, Korea.

Correspondence to: Young Do Yoo. Graduate School of Medicine, Korea University College of Medicine, 73 Inchon-ro, Seongbuk-gu, Seoul 136-705, Korea. Tel: +82-2-2286-1362, ydy1130@korea.ac.kr

Received 7 March 2013 Revised 24 April 2013 Accepted 28 April 2013

(open-access):

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Release of reactive oxygen species (ROS) generated in the mitochondria to the cytosol is well controlled by various proteins in order to maintain and regulate redox homeostasis and cellular signaling pathways, however, the exact mechanisms by which the proteins located in the mitochondrial membrane control ROS release still remains to be identified. Although there are reports that several proteins play a role in mitochondrial ROS release to the cytosol, little is known about how it is released into the cytosol or its origin. Recently, several reports demonstrated that the ROS modulator 1 (Romo1) protein located on the mitochondrial membrane modulates ROS release into the cytosol and that these ROS are indispensible for survival in both normal cells and tumor cells. If these ROS are over-produced or dysregulated in pathological conditions, they may cause oxidative damages resulting in a variety of diseases. Therefore, understanding and identifying the mechanisms by which ROS are released to the cytosol may offer new strategies for pharmaceutical therapy of diseases related to oxidative stresses.

Keywords: Reactive Oxygen Species, Mitochondria, Oxidative Stress

Figures and Tables

Fig. 1

A signaling pathway for TNF-α-induced ROS production through Romo1. TNF, tumor necrosis factor; TNF-R, TNF receptor; NF-κB, nuclear factor-kappaB; FHC, ferritin heavy chain; Mn-SOD, manganese superoxide dismutase; GADD, growth arrest and DNA-damage-inducible; A20, tumor necrosis factor inducible protein A20; XIAP, X-linked inhibitor of apoptosis protein; JNK, c-Jun N-terminal kinase; CHX, cycloheximide.

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